Hypertension and augmented vasoconstriction associated to metabolic disease have traditionally been ascribed to protein kinase-mediated Ca2+ sensitization of the VSM contractile machinery leading to increased vascular tone and systemic vascular resistance (Martínez et al., 2000; Naik et al., 2006; Villalba et al., 2007, 2011; Crestani et al., 2017). This evidence concerns the gene WEE1 and metabolic disease.